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Psoriasis PS animal model

Psoriasis PS animal model

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Psoriasis
Psychiatric & neurological disease models

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Psoriasis

Introduction to the PS Animal Model

Psoriasis is a common dermatological condition characterized by erythematous plaques covered with silvery scales on the scalp, trunk, and extremities. It tends to recur and persist, significantly impacting patients’ physical and psychological well-being. The pathogenesis of psoriasis is complex, resulting from the interplay of genetic factors, immune dysregulation, and environmental influences. Establishing an optimal animal model of psoriasis would greatly facilitate elucidation of its genetic underpinnings, pathogenic mechanisms, and the development of novel therapeutics.

Advantages of Aniphe BioLab’s PS Animal Model Platform Services

Aniphe BioLab has established a mature and comprehensive animal model platform for psoriasis, providing one-stop solutions to meet diverse pharmacological efficacy evaluation needs.

Comprehensive model coverage

A full range of models is available.

Covering a variety of classic psoriasis animal model protocols, and designed to accommodate different administration routes, including topical and oral delivery.

Standardization of the modeling process

High modeling stability

Standardized modeling procedures ensure excellent reproducibility of skin lesion phenotypes and inflammatory markers, with minimal data variability.

Multidimensional Evaluation System

End-to-end compliance management and control

Unified time-series operations and batch partition isolation ensure the integrity and traceability of raw data, while supporting regulatory submission and verification.

Adaptable to multi-cycle studies

Multi-dimensional detection and evaluation

It comprehensively integrates multiple pharmacodynamic endpoints, including skin lesion scores, histopathological sections, inflammatory cytokines, and dermatological behavioral assessments.

Adaptable to multi-cycle studies

Customized and Flexible Solutions

Experiment groups can be adjusted based on the project timeline and budget, with dedicated project coordination and follow-up.

Modeling cycle

1–2 weeks

1  Laboratory animals

C57 male mice

1  Positive drug

Commonly used topical agents include calcipotriol, dexamethasone, methotrexate, and cyclosporine A, among others.

1  Application areas

It is applied to research on the pathogenesis of psoriasis, elucidation of immune‑inflammatory pathways, evaluation of the efficacy of novel small‑molecule drugs and biologics, screening of traditional Chinese medicines and natural products, development of topical formulations, and studies on drug safety—particularly well suited for preclinical in vivo assessments of anti‑psoriasis agents targeting canonical targets such as IL‑17/IL‑23, TNF‑α, and JAK/STAT signaling.

Experimental results

PS animal model construction

Imiquimod induction: Remove the hair from the dorsal skin of the mice. Using a syringe, apply imiquimod ointment evenly to the depilated area. After application, do not place the mice back into their cages; allow 5–10 minutes for the ointment to be absorbed before returning them. Repeat this procedure daily for 5–10 consecutive days, and assess skin lesions using the PASI score each day.

The scoring criteria are as follows: The skin condition in the area treated with the medication is assessed daily, and, based on the PASI, the severity of back skin lesions (thickening, scaling, erythema) is graded on a scale from 0 to 4.

Based on the PASI, the severity of skin inflammation is assessed once daily, including measurements of skin erythema, scaling, and induration, with scores ranging from 0 to 4: 0 = none, 1 = mild, 2 = moderate, 3 = marked, and 4 = very marked.

Skin lesion images

The affected skin exhibits extensive thickening and elevation, with multiple layers of silvery-white, thick scales that are piled up in plaques. Localized erythematous patches and punctate erythema are also observed, reflecting the three hallmark features of psoriasis: scaling, infiltration, and erythema. The lesions display prominent hyperplasia and inflammatory changes, allowing for a straightforward visual assessment of lesion severity when used to grade topical or systemic therapies.

 

 

HE pathological staining analysis of skin tissue

Slices reveal typical psoriatic pathological changes: marked epidermal thickening with acanthosis and elongation of epidermal ridges; hyperkeratosis accompanied by parakeratosis, with scaling on the surface; dilated vessels in the superficial dermis and abundant inflammatory cell infiltration, fully reproducing the core histopathological features of epidermal hyperplasia and cutaneous inflammation seen in psoriasis.

 

 

 

Other induction methods

01 Cytokine Model

Currently, injecting a series of cytokines—including IL‑23, IL‑12, IL‑36, IL‑22, and IL‑17C—into the skin of mice, in combination with Oncostatin‑M and IL‑33, has been employed to induce psoriasis‑like skin inflammation. Among the various cytokine‑injection mouse models, administration of IL‑23 is the most commonly used approach; this cytokine has been injected into more than 50 distinct genetically engineered mouse models to establish disease‑relevant phenotypes.

The cytokine‑induced psoriasis model is easy to establish, can be combined with various other genetically engineered mouse models, and does not require extensive time or resources for modeling; moreover, it is relatively inexpensive. However, the psoriasis‑like skin lesions induced by this model represent an acute inflammatory response that, upon cessation of injections, gradually resolve on their own.

02 Xenograft Model

Currently, the primary recipient strains for this type of model include nude mice, severe combined immunodeficiency (SCID) mice, and AGR129 mice. Among these, nude mice were the earliest to be used for such models; SCID mice are the most widely employed; and AGR129 mice are xenograft models in which functional T cells, B cells, and NK cells are absent due to the knockout of the RAG gene.

Because it requires obtaining large amounts of untreated lesional or non-lesional skin tissue and peripheral blood from psoriasis patients, and necessitates rapid tissue collection and transplantation to prevent graft ischemia and rejection, this model has not been widely adopted.

03 Spontaneous Mutation Model

Prominent examples of spontaneously mutant mouse models include the Asebia mouse, the scaly‑skin mouse (Fsn mouse), and the chronic proliferative dermatitis mouse. These spontaneous mutants all exhibit histopathological features characteristic of psoriasis; however, T cells and neutrophils are rarely observed in their tissue sections, and they respond poorly to conventional therapies for psoriasis. As methods for generating psoriasis animal models have advanced, the use of these spontaneous mutant strains has gradually declined, and they have increasingly served as genetic backgrounds for other psoriasis‑related animal models.

04 Genetic Engineering Models

Genetically engineered mouse models account for the largest proportion among all psoriasis mouse models; currently reported genetic mouse models of psoriasis primarily include transgenic mouse models and gene-knockout mouse models.

Gene-knockout mice can be further classified into complete and partial knockouts; by completely or partially knocking out specific genes in these mice, psoriasis‑like skin lesions can be induced.

Transgenic mouse models: These models are generated by using transgenic technology to overexpress specific genes in mice, thereby inducing psoriasis‑like skin lesions. Most of these models achieve targeted gene overexpression by driving expression under the control of epidermal basal layer promoters, such as keratin 5 (K5), keratin 14 (K14), keratin 10 (K10), or involucrin, thus eliciting the development of psoriasis‑like cutaneous manifestations.

Genetically engineered animal models, from a molecular and cellular perspective, manipulate specific individual genes to induce psoriasis‑like skin pathology, thereby exhibiting high specificity. They enable the elucidation of the roles of particular genes in the pathogenesis of psoriasis and are well suited for examining the expression, function, and effects of single genes. However, these models involve complex procedures, require substantial time, and are costly, and they cannot fully replicate the intricate processes underlying human psoriasis that arise from the combined actions of multiple genes. Consequently, there remains considerable room for further research in developing transgenic animal models of psoriasis.

 

Summary

It is believed that, as research into the pathogenesis of psoriasis deepens and more disease‑related genes are identified and characterized, an increasing number of animal models—more precise in reflecting the mechanisms and clinical features of psoriasis—will emerge, thereby providing more valuable insights for elucidating its pathogenesis and developing novel therapeutic strategies.

Aniphe BioLab offers a variety of approaches for establishing psoriasis animal models and provides pharmacological and efficacy evaluation services tailored to these disease models. We welcome inquiries from all clients!